Evidence map›Paper›PMID 26308936›Full record

ArticlePloS one2015

Overexpression of Both ERG11 and ABC2 Genes Might Be Responsible for Itraconazole Resistance in Clinical Isolates of Candida krusei.

Xiaoyuan He, Mingfeng Zhao, Jinyan Chen, Rimao Wu, Jianlei Zhang, Rui Cui, Yanyu Jiang, Jie Chen, Xiaoli Cao, Yi Xing and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 30 citations in OpenAlex.

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  6. Repurposing pantoprazole and haloperidol as efflux pump inhibitors in azole resistant clinicalSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
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  17. Azole Antifungal Resistance inFrontiers in microbiology · 2016
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Xiaoyuan HeDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Mingfeng ZhaoDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Jinyan ChenDepartment of Clinical Laboratory, Tianjin First Central Hospital, Tianjin, China.
Rimao WuDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Jianlei ZhangDepartment of Clinical Laboratory, Tianjin First Central Hospital, Tianjin, China.
Rui CuiDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Yanyu JiangDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Jie ChenDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Xiaoli CaoDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Yi XingDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Yuchen ZhangDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Juanxia MengDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Qi DengDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Tao SuiDepartment of Hematology, Tianjin First Central Hospital, The First Central Clinical College of Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CNTianjin First Center Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo study the main molecular mechanisms responsible for itraconazole resistance in clinical isolates of Candida krusei.

methodsThe 14α-demethylases encoded by ERG11 gene in the 16 C.krusei clinical isolates were amplified by polymerase chain reaction (PCR), and their nucleotide sequences were determined to detect point mutations. Meanwhile, ERG11 and efflux transporters (ABC1 and ABC2) genes were determined by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) for their expression in itraconazole-resistant (R), itraconazole-susceptible dose dependent (SDD) and itraconazole-susceptible (S) C.krusei at the mRNA level.

resultsWe found 7-point mutations in ERG11 gene of all the C.krusei clinical isolates, including 6 synonymous mutations and 1 missense mutation (C44T). However, the missense mutation was found in the three groups. The mRNA levels of ERG11 gene in itraconazole-resistant isolates showed higher expression compared with itraconazole-susceptible dose dependent and itraconazole-susceptible ones (P = 0.015 and P = 0.002 respectively). ABC2 gene mRNA levels in itraconazole-resistant group was significantly higher than the other two groups, and the levels of their expression in the isolates appeared to increase with the decrease of susceptibility to itraconazole (P = 0.007 in SDD compared with S, P = 0.016 in SDD with R, and P<0.001 in S with R respectively). While ABC1 gene presented lower expression in itraconazole resistant strains. However, the mRNA levels of ERG11, ABC1 and ABC2 in a C.krusei (CK10) resistant to both itraconazole and voriconazole were expressed highest in all the itraconazole-resistant isolates.

conclusionsThere are ERG11 gene polymorphisms in clinical isolates of C.krusei. ERG11 gene mutations may not be involved in the development of itraconazole resistance in C.krusei. ERG11 and ABC2 overexpression might be responsible for the acquired itraconazole resistance of these clinical isolates.

Indexed as

Drug Resistance, FungalAntifungal AgentsATP-Binding Cassette TransportersCandidaCandidiasisFungal ProteinsGene Expression Regulation, FungalHumansItraconazoleMicrobial Sensitivity TestsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerAntifungal AgentsATP-Binding Cassette TransportersFungal ProteinsItraconazoleRNA, Messenger

Identifiers

PMID26308936
PMCPMC4550294
OpenAlexW1851369101

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.